The mechanism of inhibition by o,p'DDT and antiestrogens of the estrogen-mediated induction of uterine ornithine decarboxylase (ODC) is being investigated. The finding that there is no correlation between inhibition of ODC induction and elevation of hepatic 2-hydroxylation of estradiol indicates that these compounds do not inhibit ODC by stimulating inactivation of estradiol. The next step in attempting to explain the above mechanism will examine the possibility that inhibition of ODC is due to accumulation of polyamines. Also, the possibility that inhibition of recycling of the uterine estrogen receptor is responsible for inhibition of induction of ODC will be examined. Studies on the estrogenic or antiestrogenic activity of chlorinated hydrocarbons in DMBA-induced mammary tumors are being conducted. The question whether methoxychlor requires metabolism for estrogenic activity in vivo is being examined.